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Summary Table

Feature	Detail
Risk Factors	Nulliparity, age >35 or <20, obesity (BMI >30), chronic hypertension, diabetes mellitus, chronic kidney disease, antiphospholipid syndrome, multiple gestation, family history of preeclampsia, prior preeclampsia, molar pregnancy, autoimmune disease (SLE), assisted reproductive technology
Etiology	Abnormal placental implantation with defective spiral artery remodeling leading to placental ischemia, endothelial dysfunction, and systemic vasospasm
Patient Presentation	Elevated BP (>140/90 mmHg) after 20 weeks of gestation; headache, visual changes, RUQ or epigastric pain, facial/hand edema, sudden weight gain; may be asymptomatic and discovered on routine prenatal visit
Classic Physical Exam	Hypertension, non-dependent edema (facial, periorbital, hands), brisk deep tendon reflexes (hyperreflexia with or without clonus), RUQ tenderness, papilledema (rare but severe)
Key Diagnostic Results	Proteinuria >300 mg/24h or protein/creatinine ratio >0.3; elevated uric acid; thrombocytopenia (<100,000); elevated LDH, AST, ALT; elevated creatinine; peripheral blood smear showing schistocytes in HELLP
Management	Delivery is the definitive treatment. Labetalol or hydralazine IV for acute severe hypertension. Magnesium sulfate for seizure prophylaxis in severe preeclampsia and eclampsia. Low-dose aspirin (81 mg) for prevention in high-risk patients starting at 12 weeks.
Keywords	"New-onset hypertension after 20 weeks," "proteinuria in pregnancy," "headache and visual changes in third trimester," "RUQ pain with thrombocytopenia," "seizure in pregnant woman," "BP >160/110 with severe features," "HELLP"

1. Pathophysiology

Normal pregnancy requires extensive remodeling of the uterine spiral arteries. Cytotrophoblasts invade the spiral arteries during the first and early second trimester, replacing the muscular and elastic walls with a low-resistance, high-capacitance vascular bed. This ensures adequate uteroplacental blood flow to support the growing fetus.

In preeclampsia, this trophoblastic invasion is shallow and incomplete. The spiral arteries retain their muscular walls and remain narrow, high-resistance vessels. The result is placental ischemia and hypoperfusion. The ischemic placenta releases a cascade of antiangiogenic factors, most notably soluble fms-like tyrosine kinase 1 (sFlt-1), which binds and neutralizes circulating vascular endothelial growth factor (VEGF) and placental growth factor (PlGF). The depletion of these proangiogenic factors causes widespread maternal endothelial dysfunction.

This endothelial injury is what produces the clinical syndrome. Vasospasm throughout the maternal circulation raises systemic vascular resistance and blood pressure. Endothelial damage in the glomerulus (specifically glomerular endotheliosis, the swelling and vacuolization of glomerular endothelial cells) disrupts the filtration barrier, resulting in proteinuria. Endothelial injury in the hepatic sinusoids causes periportal necrosis and subcapsular hemorrhage, explaining the RUQ pain and elevated transaminases. Microangiopathic injury triggers platelet activation and consumption, producing thrombocytopenia. Red blood cells shearing through damaged microvasculature create schistocytes and elevate LDH, which together with thrombocytopenia and elevated liver enzymes constitute the HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets).

Cerebral endothelial dysfunction and vasospasm impair the blood-brain barrier and cerebral autoregulation. This explains the headache, visual disturbances (scotomata, blurred vision, cortical blindness from posterior reversible encephalopathy syndrome), and ultimately seizures (eclampsia). The seizures in eclampsia are thought to result from cerebral vasospasm, ischemia, and vasogenic edema rather than simply from high blood pressure alone, which is why eclampsia can occur even with only mildly elevated BP.

Understanding this pathophysiology clarifies why delivery of the placenta is the only definitive cure. All other treatments are temporizing measures that address downstream consequences without correcting the underlying placental disease.

2. Classification and Clinical Manifestation

Classification of Hypertensive Disorders in Pregnancy

Disorder	Definition	Onset	Proteinuria	Key Feature
Chronic Hypertension	BP >140/90 mmHg documented before pregnancy or before 20 weeks of gestation	Before 20 weeks	May or may not be present	Pre-existing; persists beyond 12 weeks postpartum
Gestational Hypertension	New-onset BP >140/90 mmHg after 20 weeks without proteinuria or end-organ damage	After 20 weeks	Absent	Resolves by 12 weeks postpartum; no severe features; diagnosis of exclusion
Preeclampsia without Severe Features	BP >140/90 mmHg after 20 weeks with proteinuria OR end-organ dysfunction	After 20 weeks	Present (>300 mg/24h) or end-organ criteria met	Platelets >100,000; liver enzymes normal or mildly elevated; no CNS symptoms
Preeclampsia with Severe Features	BP >160/110 mmHg OR any severe feature (see below)	After 20 weeks	May or may not be present (no longer required)	See severe features table below
Eclampsia	New-onset tonic-clonic seizures in a patient with preeclampsia that cannot be attributed to other causes	Usually third trimester, but can occur intrapartum or up to 6 weeks postpartum	Usually present	Seizures may occur without preceding severe hypertension
HELLP Syndrome	Variant of severe preeclampsia: Hemolysis + Elevated Liver enzymes + Low Platelets	Usually third trimester	May or may not be present	Can present without hypertension in up to 15% of cases
Superimposed Preeclampsia	New-onset proteinuria or sudden worsening of hypertension/new end-organ dysfunction in a patient with chronic hypertension	After 20 weeks	New or worsening	Sudden acceleration of previously stable chronic hypertension; new thrombocytopenia or elevated transaminases

Severe Features of Preeclampsia

This distinction is critical because it dictates whether expectant management is an option or whether delivery must be expedited regardless of gestational age.

Severe Feature	Criteria
Severe hypertension	Systolic BP >160 mmHg or diastolic BP >110 mmHg on two occasions at least 4 hours apart (or once if treated immediately)
Thrombocytopenia	Platelet count <100,000/microL
Hepatic dysfunction	AST or ALT >2x upper limit of normal, or severe persistent RUQ/epigastric pain unresponsive to medications
Renal insufficiency	Serum creatinine >1.1 mg/dL or doubling of baseline creatinine
Pulmonary edema	New-onset dyspnea with bilateral infiltrates
Cerebral symptoms	New-onset headache unresponsive to acetaminophen, visual disturbances (scotomata, blurred vision, cortical blindness)

HELLP Syndrome Diagnostic Criteria

Parameter	Threshold
Hemolysis	LDH >600 IU/L, elevated indirect bilirubin, schistocytes on peripheral smear, decreased haptoglobin
Elevated Liver Enzymes	AST >70 IU/L (or >2x upper limit of normal)
Low Platelets	<100,000/microL

A critical teaching point: HELLP can present with vague symptoms such as malaise, nausea, vomiting, and RUQ pain that mimic gastroenteritis, hepatitis, or cholecystitis. Approximately 15% of HELLP patients may not have hypertension, and some may lack proteinuria. This is a common exam trap. Any pregnant woman in the third trimester with RUQ pain and abnormal labs should be evaluated for HELLP regardless of her blood pressure reading.

3. Diagnostic Workup

Test	Purpose	When to Order	Key Finding
Blood pressure measurement	Screen and classify hypertension severity	Every prenatal visit; at least two readings 4 hours apart to confirm	>140/90 (hypertension); >160/110 (severe range)
Urine protein/creatinine ratio	Screen for proteinuria	Best initial test when preeclampsia suspected	>0.3 mg/mg is positive
24-hour urine protein	Quantify proteinuria (gold standard for proteinuria)	Confirmatory when spot ratio is borderline or questionable	>300 mg/24h confirms proteinuria
Urine dipstick	Rapid bedside screen	Triage/emergency	>1+ protein suggests proteinuria (high false-positive and false-negative rate; should not be used alone)
CBC with platelet count	Detect thrombocytopenia and hemolysis	All suspected preeclampsia	Platelets <100,000 = severe feature; low haptoglobin and schistocytes suggest HELLP
Comprehensive metabolic panel (AST, ALT, creatinine, LDH)	Assess liver and kidney function	All suspected preeclampsia	AST/ALT >2x normal = severe feature; Cr >1.1 = severe feature; LDH >600 suggests hemolysis
Peripheral blood smear	Confirm microangiopathic hemolytic anemia	When HELLP suspected	Schistocytes, helmet cells, burr cells
Uric acid	Supportive marker (not diagnostic)	Adjunctive	Elevated in preeclampsia due to reduced renal clearance; not used as a sole diagnostic criterion but correlates with disease severity
Coagulation studies (PT, PTT, fibrinogen)	Rule out DIC	Severe preeclampsia, HELLP, placental abruption	Prolonged PT/PTT, low fibrinogen, elevated D-dimer = DIC
Fetal assessment (NST, BPP, umbilical artery Doppler)	Evaluate fetal well-being	All confirmed preeclampsia	Nonreactive NST, low BPP score, absent/reversed end-diastolic flow indicate fetal compromise and may necessitate delivery
Ultrasound for fetal growth	Detect intrauterine growth restriction (IUGR)	Baseline at diagnosis, then serial	Estimated fetal weight <10th percentile; oligohydramnios

When a pregnant patient beyond 20 weeks presents with elevated blood pressure, the first step is to confirm the reading with at least two measurements taken 4 hours apart (unless the BP is in the severe range, in which case it can be confirmed within minutes and treated immediately).

Once hypertension is confirmed, the next step is to determine whether this is isolated gestational hypertension or preeclampsia. The best initial test to evaluate for proteinuria is a spot urine protein-to-creatinine ratio (threshold >0.3). A urine dipstick is rapid but has poor sensitivity and specificity and should not be relied upon in isolation. The 24-hour urine collection remains the gold standard for quantifying proteinuria (>300 mg/24h), but it is time-consuming and often impractical in urgent settings. In clinical practice and on exams, the spot ratio is typically acceptable.

However, proteinuria is no longer required to diagnose preeclampsia. A patient with new-onset hypertension after 20 weeks who has any end-organ dysfunction (thrombocytopenia, elevated transaminases, renal insufficiency, pulmonary edema, or cerebral/visual symptoms) meets the diagnostic criteria for preeclampsia even without proteinuria. This updated diagnostic framework is frequently tested.

After confirming preeclampsia, the next critical determination is whether severe features are present, because this directly dictates management. Order a CBC (looking for thrombocytopenia and hemolysis markers), a comprehensive metabolic panel (AST, ALT, creatinine, LDH), and assess for symptoms (headache, visual changes, RUQ pain, dyspnea). If hemolysis is suspected, add a peripheral smear, haptoglobin, and indirect bilirubin.

If the clinical picture suggests HELLP (RUQ pain, nausea/vomiting, thrombocytopenia, elevated LFTs, elevated LDH with evidence of hemolysis), coagulation studies should be sent to rule out disseminated intravascular coagulation (DIC), which can complicate HELLP and placental abruption.

Fetal surveillance with a nonstress test (NST) and biophysical profile (BPP) should be performed at diagnosis and serially thereafter. Umbilical artery Doppler velocimetry helps assess placental function, particularly in the setting of fetal growth restriction. Absent or reversed end-diastolic flow is an ominous finding that typically prompts delivery.

4. Management and Treatment

Scenario	Management	Key Details
Prevention (high-risk patients)	Low-dose aspirin 81 mg daily	Start at 12-16 weeks, continue until delivery; recommended for patients with prior preeclampsia, chronic hypertension, multifetal gestation, diabetes, renal disease, autoimmune disease
Gestational hypertension or preeclampsia without severe features, >37 weeks	Delivery	Induction of labor; vaginal delivery preferred
Preeclampsia without severe features, <37 weeks	Expectant management with close monitoring	Twice-weekly BP monitoring, weekly labs (CBC, CMP), fetal surveillance (NST 2x/week); deliver at 37 weeks or sooner if severe features develop
Preeclampsia with severe features, >34 weeks	Delivery after stabilization	Magnesium sulfate for seizure prophylaxis + antihypertensives for severe-range BP; deliver after maternal stabilization
Preeclampsia with severe features, <34 weeks	Attempt to prolong pregnancy 48 hours for corticosteroids if stable	Betamethasone 12 mg IM x2 doses 24h apart for fetal lung maturity; magnesium sulfate for seizure prophylaxis and fetal neuroprotection; deliver if maternal or fetal condition deteriorates
Preeclampsia with severe features, <24 weeks	Counseling; consider termination vs. expectant management at tertiary center	Extremely high maternal and fetal morbidity; individualized decision
Eclampsia	Magnesium sulfate + delivery	Magnesium sulfate is first-line for seizure control (NOT diazepam, NOT phenytoin); deliver after maternal stabilization regardless of gestational age
HELLP syndrome	Delivery + supportive care	Magnesium sulfate + antihypertensives; platelet transfusion if <20,000 or <50,000 before cesarean; corticosteroids do NOT reliably improve maternal outcomes in HELLP (previously used, no longer standard)
Chronic hypertension in pregnancy	Oral antihypertensives; treat when BP >140/90	First-line: labetalol, nifedipine, or methyldopa; ACE inhibitors and ARBs are absolutely contraindicated
Postpartum hypertension	Continue monitoring; oral antihypertensives as needed	Preeclampsia can develop or worsen postpartum; magnesium sulfate if severe features; NSAIDs may worsen BP

Prevention. For patients with one or more high-risk factors (prior preeclampsia, chronic hypertension, multifetal gestation, type 1 or 2 diabetes, renal disease, autoimmune disease) or two or more moderate-risk factors (nulliparity, obesity, family history, age >35, prior adverse pregnancy outcome), low-dose aspirin 81 mg daily should be started between 12 and 16 weeks of gestation and continued until delivery. Aspirin inhibits thromboxane A2 synthesis (a vasoconstrictor and platelet aggregator) while relatively preserving prostacyclin (a vasodilator), thereby improving placental perfusion. Calcium supplementation (1.5-2 g daily) is recommended in populations with low dietary calcium intake.

Acute Severe Hypertension (BP >160/110). This is a hypertensive emergency in pregnancy and requires treatment within 30-60 minutes to prevent stroke, placental abruption, and end-organ damage.

Medication	Dose	Route	Notes
Labetalol	20 mg IV initial, then 40 mg, then 80 mg every 10-20 minutes (max 300 mg total)	IV push	First-line; combined alpha and beta blocker; avoid in asthma, heart block, decompensated heart failure
Hydralazine	5 mg IV initial, then 5-10 mg IV every 20-40 minutes (max 20 mg)	IV push	Direct arteriolar vasodilator; may cause reflex tachycardia and headache (can mimic worsening preeclampsia)
Nifedipine (immediate-release)	10-20 mg PO every 20-30 minutes (max 50 mg in first hour)	Oral	Calcium channel blocker; used when IV access is not available or as an alternative; safe to use with magnesium sulfate despite older concerns

The target is to lower BP to <160/110 mmHg but not below 120/80, as aggressive reduction can compromise uteroplacental perfusion.

Seizure Prophylaxis and Treatment. Magnesium sulfate is the drug of choice for both prevention of seizures in severe preeclampsia and treatment of eclamptic seizures. It is superior to phenytoin and diazepam for this indication. The standard regimen is:

Loading dose: 4-6 g IV over 15-20 minutes
Maintenance: 1-2 g/hour continuous IV infusion
Duration: Continue for at least 24-48 hours after delivery or after the last seizure

Magnesium toxicity must be monitored closely:

Magnesium Level (mEq/L)	Clinical Effect
4-7	Therapeutic range
7-10	Loss of deep tendon reflexes
10-13	Respiratory depression
>13	Cardiac arrest

Monitor for toxicity by checking deep tendon reflexes (loss of patellar reflex is the earliest sign), respiratory rate (must remain >12/min), and urine output (must remain >25 mL/hour, as magnesium is renally excreted). The antidote for magnesium toxicity is calcium gluconate 1 g IV over 2-3 minutes.

Timing of Delivery. Delivery is the only definitive treatment for preeclampsia. The decision of when to deliver depends on gestational age and disease severity:

>37 weeks with gestational hypertension or preeclampsia without severe features: Deliver. Do not wait.
34-37 weeks without severe features: Expectant management is reasonable with close surveillance; deliver at 37 weeks.
>34 weeks with severe features: Stabilize (magnesium, antihypertensives) and deliver. No benefit to prolonging pregnancy beyond 34 weeks in severe disease.
<34 weeks with severe features: If the mother and fetus are stable, attempt to prolong pregnancy for 48 hours to administer betamethasone (12 mg IM, two doses 24 hours apart) for fetal lung maturity. Magnesium sulfate at <32 weeks also provides fetal neuroprotection against cerebral palsy. If the patient deteriorates (uncontrolled BP, eclampsia, placental abruption, DIC, nonreassuring fetal status, pulmonary edema), deliver immediately regardless of gestational age or steroid completion.

Route of Delivery. Vaginal delivery is preferred unless obstetric indications for cesarean exist. Preeclampsia alone is not an indication for cesarean section. However, in very preterm gestations with an unfavorable cervix where induction is unlikely to succeed quickly, cesarean may be chosen to minimize prolonged maternal exposure.

Contraindicated Medications. ACE inhibitors (e.g., enalapril, lisinopril) and ARBs (e.g., losartan) are absolutely contraindicated throughout pregnancy due to teratogenicity (renal agenesis, oligohydramnios, pulmonary hypoplasia, skull defects, fetal death). Nitroprusside is avoided due to fetal cyanide toxicity. Atenolol is associated with fetal growth restriction and is not preferred. Diuretics are generally avoided as they can worsen the already contracted intravascular volume in preeclampsia.

Postpartum Considerations. Preeclampsia can develop de novo or worsen in the postpartum period, particularly within the first 48-72 hours but up to 6 weeks after delivery. Patients with severe features should continue magnesium sulfate for 24-48 hours postpartum. Oral antihypertensives (labetalol, nifedipine) are used for persistent postpartum hypertension. NSAIDs should be used cautiously as they can exacerbate hypertension and are avoided in patients with renal impairment or thrombocytopenia. All patients with a history of preeclampsia carry an increased lifetime risk of cardiovascular disease and should receive long-term cardiovascular risk counseling.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Thrombotic Thrombocytopenic Purpura (TTP)	Thrombocytopenia, microangiopathic hemolytic anemia (schistocytes), elevated LDH, neurologic symptoms; overlaps heavily with HELLP/severe preeclampsia	TTP features severely low ADAMTS13 activity (<10%), fever, and predominantly neurologic symptoms (confusion, focal deficits) with relatively normal liver enzymes. HELLP has prominently elevated AST/ALT and RUQ pain. TTP does not resolve with delivery.
Hemolytic Uremic Syndrome (HUS)	Thrombocytopenia, microangiopathic hemolytic anemia, renal failure	HUS is characterized by predominant renal failure (AKI with oliguria/anuria) out of proportion to other findings. Liver enzymes are typically normal. Often triggered by Shiga toxin (diarrheal prodrome) or complement-mediated.
Acute Fatty Liver of Pregnancy (AFLP)	Third trimester; nausea, vomiting, RUQ pain, elevated liver enzymes, coagulopathy	AFLP features hypoglycemia (a hallmark finding), markedly elevated bilirubin, low fibrinogen, prolonged PT/INR (early DIC), and often a very low antithrombin III level. Platelet count may be only mildly low. AFLP is a disease of hepatic failure; HELLP is a disease of endothelial injury with hepatic involvement.
Chronic Hypertension	Elevated BP in pregnancy	Present before 20 weeks or documented pre-pregnancy; no proteinuria or end-organ dysfunction (unless superimposed preeclampsia develops); persists beyond 12 weeks postpartum
Gestational Hypertension	New BP elevation after 20 weeks	No proteinuria and no end-organ dysfunction. Diagnosis of exclusion. Up to 50% of cases diagnosed before 32 weeks will progress to preeclampsia, so close follow-up is essential.
Lupus Nephritis Flare	Proteinuria, hypertension, thrombocytopenia in a pregnant patient with SLE	Lupus flare shows low complement levels (C3, C4), elevated anti-dsDNA, active urine sediment (RBC casts), and findings in other organ systems (rash, arthritis, serositis). Complement levels are normally elevated in pregnancy, so a "normal" level may actually be depressed.
Pheochromocytoma	Paroxysmal severe hypertension; headache, diaphoresis, palpitations	Hypertension in pheochromocytoma is episodic with paroxysms, not sustained. Diagnosed by elevated fractionated plasma metanephrines or 24-hour urine catecholamines. No proteinuria or thrombocytopenia.
Antiphospholipid Syndrome (APS)	Recurrent pregnancy loss, hypertension, thrombocytopenia, can trigger preeclampsia	APS is a risk factor for preeclampsia, not a mimic. Diagnosed by persistent positive anticardiolipin antibodies, lupus anticoagulant, or anti-beta-2 glycoprotein I antibodies plus a clinical event (thrombosis or pregnancy morbidity).

6. Traps and High-Yield Pearls

The most common way students lose points on hypertension in pregnancy questions is by failing to classify the disease correctly, which leads to choosing the wrong management. The exam tests whether you can distinguish gestational hypertension from preeclampsia, and preeclampsia without severe features from preeclampsia with severe features, because each category has a different delivery threshold and treatment algorithm. If you see a pregnant patient at 35 weeks with BP of 155/100 and no other abnormalities, that is preeclampsia without severe features and you manage expectantly until 37 weeks. If you add a platelet count of 80,000 or a headache unresponsive to acetaminophen, that now becomes severe disease requiring stabilization and delivery regardless of gestational age.

A second major trap involves HELLP syndrome presenting atypically. The vignette may describe a third-trimester patient with nausea, vomiting, malaise, and RUQ pain, and the answer choices will include cholecystitis, hepatitis, or gastroenteritis. Students who do not check the labs for thrombocytopenia, hemolysis, and elevated transaminases will miss the diagnosis. Remember that HELLP can occur without hypertension or proteinuria in a notable minority of cases.

A third trap is choosing the wrong anti-seizure medication. Magnesium sulfate is the correct answer for both prophylaxis and treatment of eclamptic seizures. Phenytoin, levetiracetam, and benzodiazepines are incorrect in this context even though they are first-line anticonvulsants in other settings. The exam specifically tests whether you know that magnesium sulfate is the standard of care in pregnancy-related seizures.

Fourth, students frequently confuse HELLP with TTP or AFLP. The key discriminators to commit to memory: TTP has severely deficient ADAMTS13 and normal liver enzymes; AFLP has hypoglycemia, markedly prolonged coagulation times, and low antithrombin III; HELLP has the triad of hemolysis, elevated liver enzymes, and low platelets with improvement after delivery.

Fifth, watch for questions on postpartum preeclampsia. A patient who was normotensive during pregnancy presents 3-5 days after delivery with headache, visual changes, and BP of 170/105. This is late-onset postpartum preeclampsia and requires the same workup and treatment (magnesium sulfate, antihypertensives) as antepartum disease. Students who anchor on "delivery is the cure" forget that the disease can appear or worsen after the placenta has already been delivered.

Finally, never choose an ACE inhibitor or ARB for blood pressure management in a pregnant patient, even if it is listed as "the best antihypertensive." These are absolutely contraindicated at any gestational age. The correct oral agents are labetalol, nifedipine, or methyldopa. If the question stem mentions a patient who becomes pregnant while on lisinopril, the next best step is to discontinue the ACE inhibitor immediately and switch to a pregnancy-safe alternative.

The core competency being tested across all variations of this topic is your ability to recognize the clinical syndrome, classify the severity, and match the management to the correct category and gestational age. Every management decision branches from two questions: Does this patient have severe features? And what is the gestational age? If you can answer both, you can answer the question.

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